Abstract
The mechanism or mechanisms responsible for the arterial hypoxemia demonstrated in experimental animals (1,5,4) as well as in patients (2,3,6,7) with increased intracranial pressure (ICP) remains somewhat obscure. Intracranial pathological disorders producing chronic elevation of ICP are rarely associated with arterial hypoxemia; whereas those disorders which produce acute elevations of ICP are quite commonly associated with arterial hypoxemia. Additionally, it has been observed that those patients with increased ICP exhibiting decerebrate rigidity appeared to demonstrate this response more consistently and profoundly. This variable correlation between elevated ICP and arterial hypoxemia suggests that the observed arterial hypoxemia may not occur as a direct response or result of the elevated ICP, but is more likely a result of non-specific cardiopulmonary responses associated with ICP elevations. Thus, these investigations were designed to assess the correlation of the development of arterial hypoxemia with the rate of development of increased ICP and the severity of the associated vasopressor responses.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
